Cooperation partners of SETBP1 in AML development
Funded at Henry M. Jackson Fdn for the Adv Mil/med · NIH-11625528 · Data updated 2026-11-12
This grant explores how SETBP1 and AF9 (MLLT3) work together to drive acute myeloid leukemia and whether targeting related epigenetic regulators could help treat aggressive CK-AML.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Henry M. Jackson Fdn for the Adv Mil/med NIH-funded |
| Lab location | 1 site (Bethesda, United States) |
| Project start | September 18, 2026 |
| Project end | August 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $149,152 |
| NIH project number | 1R56CA304133-01A1 |
| Project ID | NIH-11625528 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients with acute myeloid leukemia, especially those with complex karyotype who overexpress SETBP1 and MLLT3 and may benefit from targeted epigenetic therapies.
✕Less likely to help
Patients whose AML does not involve SETBP1/MLLT3 cooperation or is not driven by the studied epigenetic regulators may not see direct benefits.
What this research studies
AML is a complex blood cancer with many patients not responding well to standard therapy. The project builds on lab findings that AF9/MLLT3 and SETBP1 cooperate to accelerate leukemia in mice and are overexpressed in a hard-to-treat CK-AML patient group. Researchers will focus on epigenetic regulators recruited by these factors to see if blocking them can hinder leukemia-related gene activation. The work aims to identify new targets that could lead to better treatments for patients with high-risk AML. Results could guide future therapies that specifically disrupt this cooperative pathway.
Why it matters
Potential benefit: If successful, this research could reveal new treatment targets for AML, potentially slowing disease progression for patients with the high-risk CK-AML subtype.
How similar studies have gone: Preclinical models have shown cooperation between SETBP1 and AF9/MLLT3 can accelerate AML, supporting the plausibility of this approach.
Where this research is happening
-
Henry M. Jackson Fdn for the Adv Mil/med
Bethesda, United States Active
Researchers
- Principal investigator: Du, Yang — Henry M. Jackson Fdn for the Adv Mil/med
- Study coordinator: Du, Yang
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.